日本科学家在11月21日出版的美国《科学》杂志上报告说，肝脏中一种蛋白质活跃可使胰腺中分泌胰岛素的贝塔细胞增殖。
胰岛素是一种具备降血糖功能的激素，由胰腺中的贝塔细胞分泌。日本东北大学教授片桐秀树领导的研究小组注意到，动物一旦肥胖，它们肝脏中的蛋白质“ERK”就会变得活跃，胰腺中贝塔细胞的数量也会相应增加。
研究人员推测“ERK”蛋白质的活跃引发贝塔细胞增殖，并通过实验证实了这一点。他们通过基因改造技术使实验鼠肝脏中的“ERK”蛋白质更容易变得活跃，结果，其胰腺中贝塔细胞的数量增加到正常值的两倍，血糖值也相应下降。
研究人员切断实验鼠肝脏和胰腺间的神经回路，然后再进行同样的实验，胰腺中的贝塔细胞便不再增殖。这证明了“ERK”蛋白质的作用通过神经传递到胰腺，最终使胰腺中的贝塔细胞增殖。
这项研究成果有望为治疗糖尿病带来新思路，但“ERK”蛋白质的活跃有引发癌症的可能，研究小组计划进一步研究能否通过刺激肝脏和胰腺间神经回路的某一部位，达到与激活“ERK”蛋白质相同的效果。（生物谷Bioon.com）
生物谷推荐原始出处：
Science 21 November 2008: DOI: 10.1126/science.1163971
Regulation of Pancreatic β Cell Mass by Neuronal Signals from the Liver
Junta Imai,1 Hideki Katagiri,2* Tetsuya Yamada,1 Yasushi Ishigaki,1 Toshinobu Suzuki,1,2 Hirohito Kudo,1,2 Kenji Uno,2 Yutaka Hasegawa,1 Junhong Gao,2 Keizo Kaneko,1,2 Hisamitsu Ishihara,1 Akira Niijima,3 Masamitsu Nakazato,4 Tomoichiro Asano,5 Yasuhiko Minokoshi,6 Yoshitomo Oka1
Metabolic regulation in mammals requires communication between multiple organs and tissues. The rise in the incidence of obesity and associated metabolic disorders, including type 2 diabetes, has renewed interest in interorgan communication. We used mouse models to explore the mechanism whereby obesity enhances pancreatic β cell mass, pathophysiological compensation for insulin resistance. We found that hepatic activation of extracellular regulated kinase (ERK) signaling induced pancreatic β cell proliferation through a neuronal-mediated relay of metabolic signals. This metabolic relay from the liver to the pancreas is involved in obesity-induced islet expansion. In mouse models of insulin-deficient diabetes, liver-selective activation of ERK signaling increased β cell mass and normalized serum glucose levels. Thus, interorgan metabolic relay systems may serve as valuable targets in regenerative treatments for diabetes.
1 Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
2 Division of Advanced Therapeutics for Metabolic Diseases, Center for Translational and Advanced Animal Research, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
3 Niigata University School of Medicine, Niigata 951-8150, Japan.
4 Third Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889-1692, Japan.
5 Department of Medical Science, Graduate School of Medicine, University of Hiroshima, Hiroshima, Japan.
6 Division of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences, Okazaki, Japan.
